Circulating epinephrine stimulates renin secretion and reduces renal sodium excretion in intact dogs, but the mechanisms involved remain unknown. Previous work indicates that these effects are mediated by beta-adrenergic receptors located extrarenally, and that changes in renal nerve activity, renal perfusion pressure, blood viscosity, and several circulating factors are not involved in the renin response. The objectives of the present proposal are to determine the mechanism(s) whereby circulating epinephrine increases renin secretion and reduces renal sodium excretion. All experiments will be conducted in anesthetized, artificially ventilated, surgically prepared dogs. In separate groups of experiments epinephrine will be infused intravenously before and after: 1) acute bilateral adrenalectomy, 2) acute thyroparathyroidectomy, 3) acute pancreatectomy, and 4) histamine receptor blockade. In addition, epinephrine will be infused directly into the carotid arteries to determine whether epinephrine-induced renin secretion is mediated by any signal originating from the head, and into the common hepatic artery to determine the role of the liver in epinephrine-induced renin secretion. Finally, the hypothesis that epinephrine-induced antinatriuresis is secondary to angiotensin II generation will be tested by comparing the sodium excretory response to intravenous epinephrine infusion before and after the administration of the converting enzyme inhibitor, SQ 20, 881, to prevent the formation of angiotensin II. These experiments will provide additional important information concerning the mechanism(s) whereby epinephrine stimulates renin secretion and reduces sodium excretion in the intact animal.